期刊
CELL
卷 167, 期 2, 页码 498-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.09.008
关键词
-
资金
- Jane Coffin Childs postdoctoral fellowship
- Human Frontiers Science Program long-term fellowship [LT000773/2010-L]
- European Molecular Biology Organization long-term fellowship [ALTF 742-2009]
- NIH [HL98316, GM62267, GM072711]
During eukaryotic DNA interstrand cross-link (ICL) repair, cross-links are resolved (unhooked'') by nucleolytic incisions surrounding the lesion. In vertebrates, ICL repair is triggered when replication forks collide with the lesion, leading to FANCI-FANCD2-dependent unhooking and formation of a double-strand break (DSB) intermediate. Using Xenopus egg extracts, we describe here a replication-coupled ICL repair pathway that does not require incisions or FANCI-FANCD2. Instead, the ICL is unhooked when one of the two N-glycosyl bonds forming the cross-link is cleaved by the DNA glycosylase NEIL3. Cleavage by NEIL3 is the primary unhooking mechanism for psoralen and abasic site ICLs. When N-glycosyl bond cleavage is prevented, unhooking occurs via FANCI-FANCD2-dependent incisions. In summary, we identify an incision-independent unhooking mechanism that avoids DSB formation and represents the preferred pathway of ICL repair in a vertebrate cell-free system.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据